Hypothesis

Cancer cell: using inflammation to invade the host

José-Ignacio Arias¹ , María-Angeles Aller² and Jaime Arias²

¹  General Surgery Unit, Monte Naranco Hospital, Oviedo, Asturias, Spain

²  Surgery I Department, School of Medicine, Complutense University of Madrid, Spain

author email corresponding author email

Molecular Cancer 2007, 6:29doi:10.1186/1476-4598-6-29

Published:	16 April 2007

Abstract

Background

Inflammation is increasingly recognized as an important component of tumorigenesis, although the mechanisms involved are not fully characterized. The invasive capacity of cancers is reflected in the classic metastatic cascade: tumor (T), node (N) and metastasis (M). However, this staging system for cancer would also have a tumoral biological significance.

Presentation of the hypothesis

To integrate the mechanisms that control the inflammatory response in the actual staging system of cancer. It is considered that in both processes of inflammation and cancer, three successive phenotypes are presented that represent the expression of trophic functional systems of increasing metabolic complexity for using oxygen.

Testing the hypothesis

While a malignant tumor develops it express phenotypes that also share the inflammatory response such as: an ischemic phenotype (anoxic-hypoxic), a leukocytic phenotype with anaerobic glycolysis and migration, and an angiogenic phenotype with hyperactivity of glycolytic enzymes, tumor proliferation and metastasis, and cachexia of the host. The increasing metabolic complexity of the tumor cell to use oxygen allows for it to be released, migrate and proliferate, thus creating structures of growing complexity.

Implication of the hypothesis

One aim of cancer gene therapy could be the induction of oxidative phosphorylation, the last metabolic step required by inflammation in order to differentiate the tissue that it produces.